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Evidence for the involvement of NOD2 in regulating colonic epithelial cell growth and survival

World Journal of Gastroenterology 2008年第38期14卷 5834-5841页

作者： Sheena M Cruickshank Louise Wakenshaw john cardone Peter D Howdle Peter J Murray Simon R Carding Molecular and Cellular Biology University of Leeds Leeds LS2 9JT United Kingdom Faculty of Life Sciences University of Manchester Manchester M13 9PT United Kingdom Institute of Molecular and Cellular Biology University of Leeds Leeds LS2 9JT United Kingdom The Institute of Food Research Norwich Research Park Norwich NR4 7UA United Kingdom Institute of Molecular and Cellular Biology University of Leeds Leeds LS2 9JT United Kingdom Section of Medicine Surgery & Anaesthesia Leeds Institute of Molecular Medicine University of Leeds Leeds LS2 9JT United Kingdom Department of Infectious Diseases St. Jude Children's Research Hospital Memphis TN 38105 United States

AIM: To investigate the function of NOD2 in colonic epithelial cells (CEC). METHODS: A combination of in vivo and in vitro analyses of epithelial cell turnover in the presence and absence of a functional NOD2 protein and, in response to enteric Salmonella typhimurium infection, were used. shRNA interference was also used to investigate the consequences of knocking down NOD2 gene expression on the growth and survival of colorectal carcinoma cell lines. RESULTS:In the colonic mucosa the highest levels of NOD2 expression were in proliferating crypt epithelial cells. Muramyl dipeptide (MDP), that is recognized by NOD2, promoted CEC growth in vitro . By contrast,the growth of NOD2-deficient CECs was impaired. In vivo CEC proliferation was also reduced and apoptosis increased in Nod2-/- mice, which were also evident following enteric Salmonella infection. Furthermore, neutralization of NOD2 mRNA expression in human colonic carcinoma cells by shRNA interference resulted in decreased survival due to increased levels of apoptosis. CONCLUSION: These findings are consistent with the involvement of NOD2 protein in promoting CEC growth and survival. Defects in proliferation by CECs in cases of CD may contribute to the underlying pathology of disrupted intestinal homeostasis and excessive inflammation.

关键词： Colon Epithelial cells NOD2 Growth

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